Molecular and Cellular Biology, May 2001, p. 3144-3158, Vol. 21, No. 9
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.9.3144-3158.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland1; Molecular Sciences Institute, Berkeley, California2; and Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas3
Received 4 December 2000/Returned for modification 17 January 2001/Accepted 8 February 2001
CTF4 and CTF18 are required for
high-fidelity chromosome segregation. Both exhibit genetic and physical
ties to replication fork constituents. We find that absence of either
CTF4 or CTF18 causes sister chromatid cohesion
failure and leads to a preanaphase accumulation of cells that depends
on the spindle assembly checkpoint. The physical and genetic
interactions between CTF4, CTF18, and core components of
replication fork complexes observed in this study and others suggest
that both gene products act in association with the replication fork to
facilitate sister chromatid cohesion. We find that Ctf18p, an
RFC1-like protein, directly interacts with Rfc2p, Rfc3p,
Rfc4p, and Rfc5p. However, Ctf18p is not a component of biochemically
purified proliferating cell nuclear antigen loading RF-C, suggesting
the presence of a discrete complex containing Ctf18p, Rfc2p, Rfc3p,
Rfc4p, and Rfc5p. Recent identification and characterization of the
budding yeast polymerase
, encoded by TRF4, strongly
supports a hypothesis that the DNA replication machinery is required
for proper sister chromatid cohesion. Analogous to the polymerase
switching role of the bacterial and human RF-C complexes, we propose
that budding yeast RF-CCTF18 may be involved in a
polymerase switch event that facilities sister chromatid cohesion. The
requirement for CTF4 and CTF18 in robust
cohesion identifies novel roles for replication accessory proteins in
this process.
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